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Our results agree with the previous reports that plasma lipid concentrations are higher among Nigerian hypertensives and diabetics than controls,16-19 and that plasma lipid concentrations are lower in this population than in Caucasians.34’35 Racial variations in plasma lipid concentrations are largely attributable to differ¬ences in the fiber component of diet. Traditional African diet is high in plant fiber and low in fats. In Rhodesia, for example, fats made up 17.8% and 42.7% of diet among Africans and whites, respectively.36 High fiber diet reduces plasma lipids through reduction of total fat intake, reduction of fat absorption, and increased bile secretion. The non-intake of cigarettes and alcohol among our patients are additional factors contributing to the comparatively lower plasma lipid concentrations obtained in the current study.
Blood pressure and glycaemic control among our patients were poor in spite of having been commenced on treatment. These observations have also been made in the recent nationwide survey of noncommunicable diseases in Nigeria. Poor blood pressure control among Nigerians has been attributed to poor compliance. suhagra 100
It is further demonstrated in this study that plasma lipid concentrations, atherogenic index and prevalence of dyslipidaemia do not differ significantly among normoglycaemic hypertensives, normotensive diabetics and type 2 diabetic hypertensives. In a recent comparative profile of patients with and those with concurrent hypertension and diabetes, total plasma cholesterol did not differ significantly between the two groups: 4.6 ±1.2 versus 4.6±0.8mmol/L.20 Another report, however, showed that the prevalence of hypercholesterolaemia was significantly higher among a population of Nigerian hypertensives with or without diabetes than those with diabetes alone: 49.3% versus 19.4%.21 This was not primarily a comparative lipid study, and confounding factors of dyslipidaemia were not excluded.
The absence of putative increases in plasma lipid concentrations in patients with concurrent type 2 diabetes and hypertension demonstrated in this study supports previous reports40’41 that neither hyperglycaemia nor elevated is responsible for hyperlipidaemia among patients with diabetes or hypertension. Specifically, dyslipidaemia does not occur in patients with secondary hypertension despite elevated blood pressure or those with insulin-like-growth factor-1 deficiency (Laron dwarf) despite persistent hyperglycemia.
Furthermore, if hypertension or diabetes influences lipid values, such values would have been magnified in the current study because of poor blood pressure and glycaemic control among our patients.
A link between diabetes, hypertension, and dyslipidaemia has been clearly described among Caucasians. In a hypertensive animal model, a defective gene was recently identified as under¬lying insulin resistance and defective fatty acid metabolism. The recognized role of genetically determined insulin resistance as a common pathogenic mechanism underlying the genesis of dyslipidaemia, diabetes, and hypertension in human metabolic syndrome may explain the lack of additive increases in plasma lipid concentrations when type 2 diabetes and hypertension occur concurrently.
Our results, therefore, appear to suggest the existence of metabolic syndrome among Nigerians. In spite of the relatively low plasma concentrations, metabolic syndrome would have important implications with respect to the potential rise in the incidence of ischaemic heart disease that has thus far been relative very low among Nigerians.
In conclusions, concurrent diabetes and hypertension does not result in excess hyperlipi-daemia than when either of the two conditions occurs in isolation. Evidence, albeit indirect, of metabolic syndrome among native Africans is provided.
We were constrained by lack of facilities for measurement of insulin and parameters of adrenergic tone such as cathecolamines in a developing country like Nigeria with scarce resources.
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